Wolff Award 1992. Exteroceptive suppression of temporalis muscle activity in patients with chronic headache and in normal volunteers: methodology, clinical and pathophysiological relevance.

Exteroceptive suppression of temporalis muscle activity was studied in patients with chronic headache and in healthy controls. Among different methods of recording, averaging 10 full-wave rectified EMG responses produces results with acceptable variability and discomfort. The late temporalis exteroceptive suppression period (ES2) is reduced on average in patients with chronic tension-type headache; this finding has been reproduced by several independent laboratories. Mean duration of temporalis ES2 is also diminished, but to a lesser degree, in daily drug abuse headache and, as shown by others, in episodic tension-type headache. It is normal in migraine between attacks, cluster headache and various types of symptomatic headaches. Temporalis ES2 may be decreased in untreated patients with major depression. In healthy volunteers, temporalis ES2 duration is reduced by a short-lasting painful stimulus to peripheral limbs after a delay of 50 to 60 ms, and by a sub-motor threshold electromagnetic stimulation to the contralateral cerebral cortex after a delay of 20 to 30 ms. In contrast, long-lasting trains of peripheral painful stimuli have no effect. Various pharmacological agents are able to modify temporalis ES2. Its duration is increased by 5-HT antagonists, but decreased by 5-HT uptake blockers. Pharmacological effects may differ between controls and patients. Considering these results and available data on the anatomo-functional organization of masticatory reflexes, we postulate that temporalis ES2 is a marker of the excitability of interneuronal nets in the ponto-medullary reticular formation. In chronic tension-type headache, excitability of these interneurons is decreased because of inadequate control by the serotonergic raphe magnus nucleus and the periaqueductal gray matter. Dysfunctioning of the latter structures might be caused by abnormal limbic inputs to the brain stem. Some steps of this pathophysiological hypothesis can be verified by modern neurophysiological techniques.